COAT platelet defect: Difference between revisions
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A '''collagen- and thrombin-activated''' (COAT) platelet defect is a [[platelet function disorder]] that is due to a reduced ability to generate [[procoagulant platelets]]. It is associated with a clinically relevant bleeding phenotype. |
A '''collagen- and thrombin-activated''' (COAT) platelet defect is a [[platelet function disorder]] that is due to a reduced ability to generate [[procoagulant platelets]]. It is associated with a clinically relevant bleeding phenotype. |
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==References== |
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Revision as of 15:44, 16 January 2022
This article relies largely or entirely on a single source. (January 2022) |
A collagen- and thrombin-activated (COAT) platelet defect is a platelet function disorder that is due to a reduced ability to generate procoagulant platelets. It is associated with a clinically relevant bleeding phenotype.
During physiological platelet activation, a fraction of platelets expresses phosphatidylserine on their surface and become highly efficient in sustaining thrombin generation. These so-called COAT platelets, can be generated by dual-agonist stimulation with collagen and thrombin in a laboratory setting. COAT platelet defects should be distinguished from Scott syndrome, a rare bleeding disorder in which patients have impaired phospholipid scrambling and do not express negatively charged phospholipids on their surface even after treatment with calcium ionophores.[1]
References
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